Publications by authors named "Bryan E Kolb"

24 Publications

  • Page 1 of 1

Bilingual experience and intrinsic functional connectivity in adults, aging, and Alzheimer's disease.

Ann N Y Acad Sci 2021 Jul 26. Epub 2021 Jul 26.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada.

The past decade marked the beginning of the use of resting-state functional connectivity (RSFC) imaging in bilingualism studies. This paper intends to review the latest evidence of changes in RSFC in language and cognitive control networks in bilinguals during adulthood, aging, and early Alzheimer's disease, which can add to our understanding of brain functional reshaping in the context of second language (L2) acquisition. Because of high variability in bilingual experience, recent studies mostly focus on the role of the main aspects of bilingual experience (age of acquisition (AoA), language proficiency, and language usage) on intrinsic functional connectivity (FC). Existing evidence accounts for stronger FC in simultaneous rather than sequential bilinguals in language and control networks, and the modulation of the AoA impact by language proficiency and usage. Studies on older bilingual adults show stronger FC in language and frontoparietal networks and preserved FC in posterior brain regions, which can protect the brain against cognitive decline and neurodegenerative processes. Altered RSFC in language and control networks subsequent to L2 training programs also is associated with improved global cognition in older adults. This review ends with a brief discussion of potential confounding factors in bilingualism research and conclusions and suggestions for future research.
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http://dx.doi.org/10.1111/nyas.14666DOI Listing
July 2021

Prenatal stress dysregulates resting-state functional connectivity and sensory motifs.

Neurobiol Stress 2021 Nov 27;15:100345. Epub 2021 May 27.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada, T1K 3M4.

Prenatal stress (PS) can impact fetal brain structure and function and contribute to higher vulnerability to neurodevelopmental and neuropsychiatric disorders. To understand how PS alters evoked and spontaneous neocortical activity and intrinsic brain functional connectivity, mesoscale voltage imaging was performed in adult C57BL/6NJ mice that had been exposed to auditory stress on gestational days 12-16, the age at which neocortex is developing. PS mice had a four-fold higher basal corticosterone level and reduced amplitude of cortical sensory-evoked responses to visual, auditory, whisker, forelimb, and hindlimb stimuli. Relative to control animals, PS led to a general reduction of resting-state functional connectivity, as well as reduced inter-modular connectivity, enhanced intra-modular connectivity, and altered frequency of auditory and forelimb spontaneous sensory motifs. These resting-state changes resulted in a cortical connectivity pattern featuring disjoint but tight modules and a decline in network efficiency. The findings demonstrate that cortical connectivity is sensitive to PS and exposed offspring may be at risk for adult stress-related neuropsychiatric disorders.
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http://dx.doi.org/10.1016/j.ynstr.2021.100345DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8173309PMC
November 2021

Prefrontal neuronal morphology in kindling-prone (FAST) and kindling-resistant (SLOW) rats.

Synapse 2021 Sep 6;75(9):e22217. Epub 2021 Jul 6.

Department of Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada.

The epileptogenic-prone (FAST) and epileptogenic-resistant (SLOW) rat strains have become a valuable tool for investigating neural plasticity. The strains were generated by breeding the rats that required the fewest amygdala stimulations to elicit a stage-5 convulsive seizure (FAST) and rats requiring the most stimulations (SLOW). Previous studies have shown differences in behavior and amygdala physiology in the two strains. This study examined the dendritic morphology of pyramidal neurons in the brains of adult male and female rats of the two strains. The brains were stained with the Golgi-Cox method and the length and branching from layer III pyramidal cells were measured in parietal cortex (Zilles Par1), medial frontal cortex (Zilles Cg3), and orbitofrontal cortex (Zilles AID) in these two strains of rats. We observed significantly longer dendrites in Cg3 in the FAST group but longer dendrites in the SLOW group in AID and Par1. There was also a sex difference (M > F) in Par1 in both strains. These morphological differences can provide insights into the neurobiological basis of the behavioral differences and suggest that localized changes in the amygdala do not occur independently of changes in other brain regions, and especially prefrontal cortex.
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http://dx.doi.org/10.1002/syn.22217DOI Listing
September 2021

Age-related hearing loss and cognitive decline: MRI and cellular evidence.

Ann N Y Acad Sci 2021 Jun 10. Epub 2021 Jun 10.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada.

Extensive evidence supports the association between age-related hearing loss (ARHL) and cognitive decline. It is, however, unknown whether a causal relationship exists between these two, or whether they both result from shared mechanisms. This paper intends to study this relationship through a comprehensive review of MRI findings as well as evidence of cellular alterations. Our review of structural MRI studies demonstrates that ARHL is independently linked to accelerated atrophy of total and regional brain volumes and reduced white matter integrity. Resting-state and task-based fMRI studies on ARHL also show changes in spontaneous neural activity and brain functional connectivity; and alterations in brain areas supporting auditory, language, cognitive, and affective processing independent of age, respectively. Although MRI findings support a causal relationship between ARHL and cognitive decline, the contribution of potential shared mechanisms should also be considered. In this regard, the review of cellular evidence indicates their role as possible common mechanisms underlying both age-related changes in hearing and cognition. Considering existing evidence, no single hypothesis can explain the link between ARHL and cognitive decline, and the contribution of both causal (i.e., the sensory hypothesis) and shared (i.e., the common cause hypothesis) mechanisms is expected.
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http://dx.doi.org/10.1111/nyas.14617DOI Listing
June 2021

Hearing Loss, Tinnitus, and Dizziness in COVID-19: A Systematic Review and Meta-Analysis.

Can J Neurol Sci 2021 Apr 12:1-12. Epub 2021 Apr 12.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Canada.

Objectives: Extensive studies indicate that severe acute respiratory syndrome coronavirus (SARS-CoV-2) involves human sensory systems. A lack of discussion, however, exists given the auditory-vestibular system involvement in CoV disease 2019 (COVID-19). The present systematic review and meta-analysis were performed to determine the event rate (ER) of hearing loss, tinnitus, and dizziness caused by SARS-CoV-2.

Methods: Databases (PubMed, ScienceDirect, Wiley) and World Health Organization updates were searched using combined keywords: 'COVID-19,' 'SARS-CoV-2,' 'pandemic,' 'auditory dysfunction,' 'hearing loss,' 'tinnitus,' 'vestibular dysfunction,' 'dizziness,' 'vertigo,' and 'otologic symptoms.'

Results: Twelve papers met the eligibility criteria and were included in the study. These papers were single group prospective, cross-sectional, or retrospective studies on otolaryngologic, neurologic, or general clinical symptoms of COVID-19 and had used subjective assessments for data collection (case histories/medical records). The results of the meta-analysis demonstrate that the ER of hearing loss (3.1%, CIs: 0.01-0.09), tinnitus (4.5%, CIs: 0.012-0.153), and dizziness (12.2%, CIs: 0.070-0.204) is statistically significant in patients with COVID-19 (Z ≤ -4.469, p ≤ 0.001).

Conclusions: COVID-19 can cause hearing loss, tinnitus, and dizziness. These findings, however, should be interpreted with caution given insufficient evidence and heterogeneity among studies. Well-designed studies and follow-up assessments on otologic symptoms of SARS-CoV-2 using standard objective tests are recommended.
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http://dx.doi.org/10.1017/cjn.2021.63DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267343PMC
April 2021

Traffic noise exposure, cognitive decline, and amyloid-beta pathology in an AD mouse model.

Synapse 2021 Apr 3;75(4):e22192. Epub 2020 Nov 3.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada.

Concerns are growing that exposure to environmental pollutants, such as traffic noise, might cause cognitive impairments and predispose individuals toward the development of Alzheimer's disease (AD) dementia. In this study in a knock-in mouse model of AD, we investigated how chronic traffic noise exposure (CTNE) impacts cognitive performance and amyloid-beta (Aβ) pathology. A group of APP mice was exposed to CTNE (70 dB , 8 hr/day for 1 month) and compared with nonexposed counterparts. Following CTNE, an increase in hypothalamic-pituitary-adrenal (HPA) axis responsivity was observed by corticosterone assay of the blood. One month after CTNE, the CTNE group demonstrated impairments in cognitive and motor functions, and indications of anxiety-like behavior, relative to the control animals. The noise-exposed group also showed elevated Aβ aggregation, as inferred by a greater number of plaques and larger average plaque size in various regions of the brain, including regions involved in stress regulation. The results support that noise-associated dysregulation of the neuroendocrine system as a potential risk factor for developing cognitive impairment and Aβ pathology, which should be further investigated in human studies.
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http://dx.doi.org/10.1002/syn.22192DOI Listing
April 2021

Noise Damage Accelerates Auditory Aging and Tinnitus: A Canadian Population-Based Study.

Otol Neurotol 2020 12;41(10):1316-1326

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada.

Objective: Age-related hearing loss (ARHL) is the third most challenging disability in older adults. Noise is a known modifiable risk factor of ARHL, which can drive adverse health effects. Few large-scale studies, however, have shown how chronic noise exposure (CNE) impacts the progression of ARHL and tinnitus.

Study Design: Retrospective large-scale study.

Setting: Audiology clinical practice.

Patients: In this study, 928 individuals aged 30-100 years without (n=497) or with the experience of CNE (n=431) were compared in their hearing assessments and tinnitus. In order to only investigate the impact of CNE on ARHL and tinnitus, people with other risk factors of hearing loss were excluded from the study.

Intervention: Diagnostic.

Main Outcome Measures: Noise damage was associated with a greater ARHL per age decades (pure-tone average(PTA)0.5-4kHz alterations 19.6-70.8 dB vs. 8.0-63.2 dB, ≤0.001), an acceleration of developing a significant ARHL at least by two decades (PTA0.5-4kHz 33.4 dB at 50-59yr vs. 28.2 dB at 30-39yr, ≤0.001), and an increased loss of word recognition scores (total average 84.7% vs. 80.0%, ≤0.001). Significant noise-associated growth in the prevalence of tinnitus also was shown, including more than a triple prevalence for constant tinnitus (28.10% vs. 8.85%, ≤0.001) and near to a double prevalence for intermittent tinnitus (19.10% vs. 11.10%, ≤0.001). Noise also resulted in the elevation of the static compliance of the tympanic membrane throughout age (total average 0.61 vs. 0.85 mmho, ≤0.001).

Conclusions: Our findings emphasize the significant contribution of CNE in auditory aging and the precipitation of both ARHL and tinnitus.
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http://dx.doi.org/10.1097/MAO.0000000000002848DOI Listing
December 2020

Reply to a Letter by Dr. Stefani and Colleagues on: "Auditory Dysfunction in Parkinson's Disease".

Mov Disord 2020 07;35(7):1284-1285

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada.

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http://dx.doi.org/10.1002/mds.28133DOI Listing
July 2020

Neural oscillations and brain stimulation in Alzheimer's disease.

Prog Neurobiol 2020 11 29;194:101878. Epub 2020 Jun 29.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada. Electronic address:

Aging is associated with alterations in cognitive processing and brain neurophysiology. Whereas the primary symptom of amnestic mild cognitive impairment (aMCI) is memory problems greater than normal for age and education, patients with Alzheimer's disease (AD) show impairments in other cognitive domains in addition to memory dysfunction. Resting-state electroencephalography (rsEEG) studies in physiological aging indicate a global increase in low-frequency oscillations' power and the reduction and slowing of alpha activity. The enhancement of slow and the reduction of fast oscillations, and the disruption of brain functional connectivity, however, are characterized as major rsEEG changes in AD. Recent rodent studies also support human evidence of age- and AD-related changes in resting-state brain oscillations, and the neuroprotective effect of brain stimulation techniques through gamma-band stimulations. Cumulatively, current evidence moves toward optimizing rsEEG features as reliable predictors of people with aMCI at risk for conversion to AD and mapping neural alterations subsequent to brain stimulation therapies. The present paper reviews the latest evidence of changes in rsEEG oscillations in physiological aging, aMCI, and AD, as well as findings of various brain stimulation therapies from both human and non-human studies.
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http://dx.doi.org/10.1016/j.pneurobio.2020.101878DOI Listing
November 2020

Prepulse inhibition of the acoustic startle reflex and P50 gating in aging and alzheimer's disease.

Ageing Res Rev 2020 05 21;59:101028. Epub 2020 Feb 21.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, T1K 3M4 AB, Canada. Electronic address:

Inhibition plays a crucial role in many functional domains, such as cognition, emotion, and actions. Studies on cognitive aging demonstrate changes in inhibitory mechanisms are age- and pathology-related. Prepulse inhibition (PPI) is the suppression of an acoustic startle reflex (ASR) to an intense stimulus when a weak prepulse stimulus precedes the startle stimulus. A reduction of PPI is thought to reflect dysfunction of sensorimotor gating which normally suppresses excessive behavioral responses to disruptive stimuli. Both human and rodent studies show age-dependent alterations of PPI of the ASR that are further compromised in Alzheimer's disease (AD). The auditory P50 gating, an index of repetition suppression, also is characterized as a putative electrophysiological biomarker of prodromal AD. This review provides the latest evidence of age- and AD-associated impairment of sensorimotor gating based upon both human and rodent studies, as well as the AD-related disruption of P50 gating in humans. It begins with a concise review of neural networks underlying PPI regulation. Then, evidence of age- and AD-related dysfunction of both PPI and P50 gating is discussed. The attentional/ emotional aspects of sensorimotor gating and the neurotransmitter mechanisms underpinning PPI and P50 gating are also reviewed. The review ends with conclusions and research directions.
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http://dx.doi.org/10.1016/j.arr.2020.101028DOI Listing
May 2020

Auditory Dysfunction in Parkinson's Disease.

Mov Disord 2020 04 13;35(4):537-550. Epub 2020 Feb 13.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada.

PD is a progressive and complex neurological disorder with heterogeneous symptomatology. PD is characterized by classical motor features of parkinsonism and nonmotor symptoms and involves extensive regions of the nervous system, various neurotransmitters, and protein aggregates. Extensive evidence supports auditory dysfunction as an additional nonmotor feature of PD. Studies indicate a broad range of auditory impairments in PD, from the peripheral hearing system to the auditory brainstem and cortical areas. For instance, research demonstrates a higher occurrence of hearing loss in early-onset PD and evidence of abnormal auditory evoked potentials, event-related potentials, and habituation to novel stimuli. Electrophysiological data, such as auditory P3a, also is suggested as a sensitive measure of illness duration and severity. Improvement in auditory responses following dopaminergic therapies also indicates the presence of similar neurotransmitters (i.e., glutamate and dopamine) in the auditory system and basal ganglia. Nonetheless, hearing impairments in PD have received little attention in clinical practice so far. This review summarizes evidence of peripheral and central auditory impairments in PD and provides conclusions and directions for future empirical and clinical research. © 2020 International Parkinson and Movement Disorder Society.
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http://dx.doi.org/10.1002/mds.28000DOI Listing
April 2020

Age-related hearing loss and tinnitus, dementia risk, and auditory amplification outcomes.

Ageing Res Rev 2019 12 23;56:100963. Epub 2019 Sep 23.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada. Electronic address:

Age-related hearing loss (ARHL) or presbycusis, as the third leading cause of chronic disability in older adults, has been shown to be associated with predisposing cognitive impairment and dementia. Tinnitus is also a chronic auditory disorder demonstrating a growth rate with increasing age. Recent evidence stands for the link between bothersome tinnitus and impairments in various aspects of cognitive function. Both ARHL and age-related tinnitus affect mental health and contribute to developing anxiety, stress, and depression. The present review is a comprehensive multidisciplinary study on diverse interactions among ARHL, tinnitus, and cognitive decline in older adults. This review incorporates the latest evidence in prevalence and risk factors of ARHL and tinnitus, the neural substrates of tinnitus-related cognitive impairments, hypothesized mechanisms concerning the association between ARHL and increased risk of dementia, hearing amplification outcomes in cases with ARHL and cognitive decline, and preliminary findings on the link between ARHL and cognitive impairment in animal studies. Given extensive evidence that demonstrates advantages of using auditory amplification in the alleviation of hearing handicap, depression, and tinnitus, and the improvement of cognition, social communication, and quality of life, regular hearing screening programs for identification and management of midlife hearing loss and tinnitus is strongly recommended.
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http://dx.doi.org/10.1016/j.arr.2019.100963DOI Listing
December 2019

Life-Course Contribution of Prenatal Stress in Regulating the Neural Modulation Network Underlying the Prepulse Inhibition of the Acoustic Startle Reflex in Male Alzheimer's Disease Mice.

Cereb Cortex 2020 01;30(1):311-325

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada.

The prepulse inhibition (PPI) of the acoustic startle reflex (ASR), as an index of sensorimotor gating, is one of the most extensively used paradigms in the field of neuropsychiatric disorders. Few studies have examined how prenatal stress (PS) regulates the sensorimotor gating during the lifespan and how PS modifies the development of amyloid-beta (Aβ) pathology in brain areas underlying the PPI formation. We followed alternations in corticosterone levels, learning and memory, and the PPI of the ASR measures in APPNL-G-F/NL-G-F offspring of dams exposed to gestational noise stress. In-depth quantifications of the Aβ plaque accumulation were also performed at 6 months. The results indicated an age-dependent deterioration of sensorimotor gating, long-lasting PS-induced abnormalities in PPI magnitudes, as well as deficits in spatial memory. The PS also resulted in a higher Aβ aggregation predominantly in brain areas associated with the PPI modulation network. The findings suggest the contribution of a PS-induced hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in regulating the PPI modulation substrates leading to the abnormal development of the neural protection system in response to disruptive stimuli. The long-lasting HPA axis dysregulation appears to be the major underlying mechanism in precipitating the Aβ deposition, especially in brain areas contributed to the PPI modulation network.
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http://dx.doi.org/10.1093/cercor/bhz089DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7029700PMC
January 2020

Noise exposure accelerates the risk of cognitive impairment and Alzheimer's disease: Adulthood, gestational, and prenatal mechanistic evidence from animal studies.

Neurosci Biobehav Rev 2020 10 9;117:110-128. Epub 2019 Apr 9.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada. Electronic address:

This review examines the adverse impacts of different noise exposure paradigms on the neuroendocrine system, hippocampal and neocortical structures, cognitive performances, and the development of Alzheimer's disease (AD)-like neuropathological changes in the brain of laboratory animals. Studies were reviewed in three periods during the lifespan including: adult animals exposed to noise, female rodents exposed to noise during gestation, and offspring exposed to noise during the prenatal period. Findings imply that chronic noise exposure dysregulates the neuroendocrine system leading to hyperactivation of the sympathetic divisions of the autonomic nervous system (i.e., the hypothalamic-pituitary-adrenal (HPA)-axis), and increases stress hormones that affect brain and behaviour. Enduring dysregulation of the HPA-axis was the most discussed mechanism for the harmful effect of noise during the lifespan. Studies also suggest a causative association of noise with diverse indicators of the AD-like neuropathology in rodents and a hypersusceptibility in females. The results indicate the importance of future neuroimaging studies to quantify the potential contribution of noise in predisposing cognitive decline and preclinical signs of dementia in humans.
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http://dx.doi.org/10.1016/j.neubiorev.2019.04.001DOI Listing
October 2020

Prenatal noise stress aggravates cognitive decline and the onset and progression of beta amyloid pathology in a mouse model of Alzheimer's disease.

Neurobiol Aging 2019 05 30;77:66-86. Epub 2019 Jan 30.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience (CCBN), University of Lethbridge, Lethbridge, Alberta, Canada. Electronic address:

Environmental distresses occurring during the sensitive periods of early life may exacerbate the vulnerability to develop physical and mental diseases in old age. Studies have shown the impact of prenatal stress (PS) on the endocrine development and reprogramming of hypothalamic-pituitary-adrenal axis functions in association with cognitive development and susceptibility to neuropsychiatric diseases. Long-term exposure to glucocorticoids can damage the brain and intensify the progression of Alzheimer's disease (AD)-like neuropathological changes, especially in females. There is, however, less information as to the link between PS and the risk of developing AD pathology throughout the lifespan. In the present study, male and female APP offspring of dams exposed to gestational noise stress were compared with the control offspring in corticosterone alternations, cognitive and motor performances, and the onset age and development of amyloid beta (Aβ) plaques across age. The hyperactivity of the hypothalamic-pituitary-adrenal axis, spatial learning, and Aβ development were sex specific, showing persistent high levels of stress and further memory loss in females than males, especially in PS mice. The Aβ deposition was started earlier, by 2-3 months, and exhibited a heightened progression in PS animals. The PS also created a long-lasting anxiety-like behavior and impairment in cognitive function and motor coordination. Our results suggested PS as a risk to exacerbate AD-like neuropathological changes during the lifespan, with higher susceptibility of females. The findings were discussed in line with the most likely mechanisms for the PS effects, that is, dysregulation of the neuroendocrine system and the placenta by the PS.
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http://dx.doi.org/10.1016/j.neurobiolaging.2019.01.019DOI Listing
May 2019

Gestational Stress Augments Postpartum β-Amyloid Pathology and Cognitive Decline in a Mouse Model of Alzheimer's Disease.

Cereb Cortex 2019 08;29(9):3712-3724

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience (CCBN), University of Lethbridge, Lethbridge, Canada.

Besides well-known risk factors for Alzheimer's disease (AD), stress, and in particular noise stress (NS), is a lifestyle risk factor common today. It is known that females are at a significantly greater risk of developing AD than males, and given that stress is a common adversity in females during pregnancy, we hypothesized that gestational noise exposure could exacerbate the postpartum development of the AD-like neuropathological changes during the life span. Pregnant APPNL-G-F/NL-G-F mice were randomly assigned to either the stress condition or control group. The stress group was exposed to the NS on gestational days 12-16, which resulted in a markedly higher hypothalamic-pituitary-adrenal (HPA) axis responsivity during the postpartum stage. Higher amyloid-β (Aβ) deposition and larger Aβ plaque size in the olfactory area were the early onset impacts of the gestational stress (GS) seen at the age of 4 months. This pattern of increased Aβ aggregation and larger plaque size were observed in various brain areas involved in both AD and stress regulation, especially in limbic structures, at the age of 6 months. The GS also produced anxiety-like behavior, deficits in learning and memory, and impaired motor coordination. The findings suggest that environmental stresses during pregnancy pose a potential risk factor in accelerating postpartum cognitive decline and AD-like neuropathological changes in the dams (mothers) later in life.
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http://dx.doi.org/10.1093/cercor/bhy251DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6686749PMC
August 2019

Chronic traffic noise stress accelerates brain impairment and cognitive decline in mice.

Exp Neurol 2018 10 22;308:1-12. Epub 2018 Jun 22.

Department of Neuroscience, Canadian Center for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB T1K 3M4, Canada. Electronic address:

Although traffic noise exposure is a well-known environmental pollutant whose negative health effect has been discussed in different aspects of the human life, only a few animal studies have tackled this issue as a cohort study, which is not feasible to be addressed in human studies. In addition to the deleterious impact of the daytime noise on well-being, chronic nocturnal noise can also disturb sleep and affects physical and mental health, but to date, little research has examined the neurobiological effects of light/dark cycles of traffic noise exposure. We investigated the effects of light/dark cycles and sex on the impact of chronic traffic noise exposure on mouse brain structure-function. The mice were randomly assigned to either one of two stress conditions or a control condition. Animals were exposed to traffic noise on either the light-cycle (LC) or dark-cycle (DC) for 30 days. Traffic noise exposure caused the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, anxiety-like behavior, impairments in learning and memory, dysfunction in balance and motor coordination, and a reduction in variety of brain measures including a brain volume, medial prefrontal cortex (mPFC) area, cortical thickness, hippocampal volume, amygdala area, and the neural density in mPFC and dentate gyrus. All behavioral and brain measures revealed adverse effects of the chronic noise stress irrespective of the LC/DC exposure or sex. Our findings were a re-emphasis on the significance of noise prevention and mitigation strategies for public health.
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http://dx.doi.org/10.1016/j.expneurol.2018.06.011DOI Listing
October 2018

Prenatal noise stress impairs HPA axis and cognitive performance in mice.

Sci Rep 2017 09 5;7(1):10560. Epub 2017 Sep 5.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience (CCBN), University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada.

Noise stress is a common environmental pollutant whose adverse effect on offspring performance has been less studied. This study was novel in terms of using "noise" as a prenatal stress compared with physical stress to explore the effect of stress during gestation on HPA axis activation, cognitive performance, and motor coordination, as well as in investigating the effect of behavioral assessments on the corticosterone (CORT) levels. Three groups of C57BL/6 mice with a gestational history of either noise stress (NS), physical stress (PS), or no stress were examined in several behavioral tests. Plasma CORT level was significantly higher before starting the behavioral tests in NS group than the two other groups. It was significantly increased after the behavioral tests in both prenatal stressed groups relative to the controls. Stress caused anxiety-like behavior and reduced learning and memory performance in both stressed groups compared to the controls, as well as decreased motor coordination in the NS group relative to the other groups. The findings suggested that: prenatal NS severely changes the HPA axis; both prenatal stressors, and particularly NS, negatively impair the offspring's cognitive and motor performance; and, they also cause a strong susceptibility to interpret environmental experiences as stressful conditions.
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http://dx.doi.org/10.1038/s41598-017-09799-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5585382PMC
September 2017

Corticosterone response to gestational stress and postpartum memory function in mice.

PLoS One 2017 10;12(7):e0180306. Epub 2017 Jul 10.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience (CCBN), University of Lethbridge, Lethbridge, AB, Canada.

Maternal stress is a common adversity during pregnancy. Gestational corticosterone alternations are thought to contribute to the etiology of postpartum behavioral disturbances. However, the impact of stress during pregnancy, in particular noise exposure, on gestational corticosterone fluctuations and spatial cognition in postpartum mice has not been fully understood yet. We hypothesized that noise exposure during pregnancy negatively affects gestational corticosterone levels and postpartum memory function in the dams similar to the physical stressors. Pregnant C57BL/6 mice were randomly assigned to either one of two stress conditions or a control condition. The noise stress (NS) was induced by presenting a loud intermittent 3000 Hz frequency on gestational days (GDs) 12, 14, and 16 for 24 hours, whereas the physical stress (PS) consisted of restraint and exposure to an elevated platform on GDs 12-16. Plasma corticosterone level was collected on GDs 11 and 17, and Morris water task (MWT) was carried out 30 days after parturition. Compared to the control group, the level of corticosterone in the stressed groups was significantly increased on GD17 relative to GD11. Significantly longer swim time and lower swim speed were observed in both stressed groups relative to the control group. Probe time was significantly shorter in the NS group than the other groups. The delta corticosterone level was significantly correlated with the swim time as well as the probe time in the three groups. Given the results, the adverse effects of gestational noise exposure on the hypothalamic pituitary-adrenal (HPA) axis activation and postpartum spatial learning and memory function were as large as/ or a bit stronger than the physical stresses. The findings suggest the significance of conservation against loud noise exposure in daily living, as well as need to further notice to the different aspects of gestational stress in mothers' behavior like offspring.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0180306PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503237PMC
September 2017

The Adverse Effects of Auditory Stress on Mouse Uterus Receptivity and Behaviour.

Sci Rep 2017 07 5;7(1):4720. Epub 2017 Jul 5.

Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada.

Stress during gestation has harmful effects on pregnancy outcome and can lead to spontaneous abortion. Few studies, however, have addressed the impact of gestational stress, particularly auditory stress, on behavioural performance and pregnancy outcome in mice. This study aimed to examine the effect of two types of gestational stress on uterus receptivity and behavioural performance. Pregnant C57BL/6 mice were randomly assigned to either auditory or physical stress conditions or a control condition from gestational days 12-16. The auditory stress regimen used loud 3000 Hz tone, while the physical stressor consisted of restraint and exposure to an elevated platform. Three behavioural tests were performed in the dams after weaning. Uterine receptivity was investigated by counting the number of sites of implantation and fetal resorption. Also, the offspring survival rates during the early postnatal period were calculated. Auditory stress caused an increase in anxiety-like behaviour, reduced time spent exploring new object/environment, and reduced balance when compared to the physical stress and control groups. Auditory stress also caused higher rates of resorbed embryos and reduction of litter size. Our results suggest that the adverse effect of noise stress is stronger than physical stress for both uterus receptivity and behavioural performance of the dams.
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http://dx.doi.org/10.1038/s41598-017-04943-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5498668PMC
July 2017

Effect of acute stress on auditory processing: a systematic review of human studies.

Rev Neurosci 2017 01;28(1):1-13

Stress is an integral part of modern life. Although there is a large body of literature regarding the harmful effects of chronic stress on different aspects of human life, acute stress is the most common form of stress, resulting from the demands and pressures of the recent past and the anticipated demands and pressures of the near future. In spite of its pervasive nature, less attention has been paid to the impact of acute stress on sensory processing than to the consequences of chronic stress, particularly concerning auditory processing. In this systematic review, the impact of experimental acute stress on the auditory processing of healthy adults was investigated. The results revealed the adverse effects of acute physical and psychological stresses on auditory processing. According to the open field of research on stress and the auditory system and the high possibility of experiencing different types of acute stresses in various life environments, including testing places, it seems that more investigations are needed to identify and manage different types of acute stresses in both clinical and research situations.
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http://dx.doi.org/10.1515/revneuro-2016-0043DOI Listing
January 2017

Learning-induced alterations in prefrontal cortical dendritic morphology.

Behav Brain Res 2010 Dec 28;214(1):91-101. Epub 2010 Apr 28.

Canadian Center for Behavioral Neuroscience, University of Lethbridge, Lethbridge, T1K 3M4, Canada.

The influences of complex housing, T-maze, and Grice box training on dendritic morphology of the prefrontal cortex (PFC) and primary somatosensory (Par 1) were investigated in the rat. Golgi-Cox analyses demonstrated that all learning paradigms produced alterations in PFC connectivity, albeit differently. Furthermore, the effects of experience on dendritic morphology varied by region, hemisphere, and lamina and often resulted in opposing changes within each. For example, complex housing produced a time-dependent decrease in the dendritic fields of layer (L) V neurons in region 3 of the cingulate cortex (Cg3) in the medial PFC (mPFC) neurons and increases in LIII of the dorsal agranular insular (AID) region of the orbitofrontal cortex. In contrast, T-maze training produced increases in Cg3 LV and decreases in AID LIII spine density. Of interest, the influence of experience was not reflected equally between hemispheres. For example, T-maze training produced an increase in Cg3 LV and AID LIII branch order and length in the right hemisphere, and an increase in Cg3 LIII branch order in the left hemisphere. Additionally, correlation analysis of task performance and dendritic morphology indicated an opposing influence of experience within the different laminae of the Cg3. For example, whereas, performance was negatively correlated with Cg3 LV dendritic branch order/length, there was a positive correlation with Cg3 LIII dendrites. Complex housing induced changes in the Par 1were also time -dependent but were only apparent after a prolonged period of exposure. In addition to demonstrating learning-specific modifications in dendritic connectivity within the PFC, the results illustrate varying patterns of change that likely reflect task-dependent requirements on the PFC.
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http://dx.doi.org/10.1016/j.bbr.2010.04.033DOI Listing
December 2010

Tactile stimulation promotes motor recovery following cortical injury in adult rats.

Behav Brain Res 2010 Dec 13;214(1):102-7. Epub 2010 Apr 13.

Canadian Centre for Behavioral Neuroscience, The University of Lethbridge, Alberta, Canada.

Tactile stimulation has been reported to be effective as a treatment for inducing growth in premature human babies and infant rats and for improving functional recovery after brain injury in infant rats. We wondered if the behavioral impairments following injury in adulthood would show similar improvements with tactile stimulation. To test this hypothesis, rats were given either bilateral medial frontal cortex aspiration lesions or a unilateral focal stroke produced in the sensorimotor cortex using the pial stripping technique. In both conditions, rats that were designated to the tactile stimulation treatment group received the stimulation for one week before the surgery to accustom them to the stimulation procedure and then two weeks postoperatively. After a three-week recovery period, the animals with frontal damage were tested in a tray-reaching task. Animals with sensorimotor cortex damage were tested in a single pellet reaching task. Following behavioral testing brains were processed for Golgi-Cox analyses. Marked improvement was found in motor performance in the lesion-tactile stimulation animals regardless of the nature of the cortical injury. The observed behavioral recovery was associated with an increase in dendritic length in pyramidal cells adjacent cortex in the frontal operates and in the intact sensorimotor cortex in the stroke animals. Taken together, these data show tactile stimulation can improve motor performance in adult animals and the improvement is correlated with dendritic sprouting. This finding could have implications for therapy in humans following stroke.
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http://dx.doi.org/10.1016/j.bbr.2010.04.008DOI Listing
December 2010

Dendritic plasticity in the adult rat following middle cerebral artery occlusion and Nogo-a neutralization.

Cereb Cortex 2006 Apr 20;16(4):529-36. Epub 2005 Jul 20.

Research, Hines VA Hospital, Hines, IL 60141, USA.

Our work has shown that following focal ischemic lesion in adult rats, neutralization of the axon growth inhibitor Nogo-A with the monoclonal antibody (mAb) IN-1 results in functional recovery. Furthermore, new axonal connections were formed from the contralesional cortex to subcortical areas corresponding to the observed functional recovery. The present study investigated whether dendritic changes, also known to subserve functional recovery, paralleled the axonal plasticity shown after ischemic lesion and treatment with mAb IN-1. Golgi-Cox-stained layer V pyramidal neurons in the contralesional sensorimotor cortex were examined for evidence of dendritic sprouting. Results demonstrated increased dendritic arborization and spine density in the mAb IN-1-treated animals with lesion. Interestingly, administration of mAb IN-1 without lesion resulted in transient dendritic outgrowth with no change in spine density. These results suggest a novel role for Nogo-A in limiting dendritic plasticity after stroke.
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http://dx.doi.org/10.1093/cercor/bhi132DOI Listing
April 2006
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